Cardiac tamponade is caused by the accumulation of fluid under pressure in the pericardial space. Despite an increase in heart rate and venous pressures, cardiac output decreases continuously as intrapericardial pressure (IPP) increases. As tamponade progresses, heart size decreases and the relative sizes of the chambers fluctuate depending on the phase of respiration. Abrupt collapse of portions of the atria and later the right ventricle occur and pulsus paradoxus increases. Although there is agreement concerning these events, there is no clear understanding of the hemodynamic mechanism(s) responsible. Cardiac tamponade is an important condition which if not recognized and treated promptly, is fatal. A better understanding of the pathophysiology of cardiac tamponade will lead to improvements in diagnosis and therapy. We will test the hypothesis that when IPP exceeds ventricular filling pressures during cardiac tamponade, the compliant chambers of the heart begin to act as Starling resistors, severely restricting cardiac filling and making it more sensitive to the effects of respiration and increasing heart rate. When pressure surrounding them exceeds downstream pressure, Starling resistors adjust their shape so that flow is relatively independent of the difference between inlet and downstream pressures until a critical value of flow is reached. Our preliminary studies show that both the right and left heart function as two compliance Starling resistors. We will begin by studying well controlled simple systems and proceed to our chronic canine model of cardiac tamponade. We will test the hypotheses that during cardiac tamponade: 1) when IPP exceeds downstream pressure a Starling resistor mechanism begins to influence both right and left ventricular filling resulting in slower rates of filling and chamber collapse, 2) the decrease in cardiac output occurs because a) the pressure difference favoring filling and thus the rate of filling decreases, and b) the time available for filling declines as heart rate increases, 3) the length of the resistor in the right heart decreases as filling progresses from the outflow tract to the atrium, 4) the Starling resistor mechanism results in a low amplitude monophasic tricuspid and mitral blood flow waveform with little change produced by atrial contraction, 5) the left atrial Starling resistor dominates left heart filling because the left ventricle is relatively noncompliant, and 6) the left atrial Starling resistor produces wide swings in the pressure difference favoring flow into the left ventricle and leads to pulsus paradoxus. When left ventricular diastolic pressures exceed IPP the conditions necessary for the creation of a Starling resistor are not met, thus accounting for the absence of pulsus paradoxus in the presence of left ventricular failure and aortic insufficiency. This series of experiments is important because it will provide a unifying explanation for many clinical observations and can fundamentally change our understanding of the pathophysiology of cardiac tamponade.